Skip to content
Open access

755. Educational attainment–related genetic and structural divergences between schizophrenia and bipolar disorder

Sep 2026 · International Journal of Neuropsychopharmacology · Vol 29, pp. i66 - i66 · 0 citations

Abstract

Abstract Background Schizophrenia (SCZ) and bipolar disorder (BD) share substantial genetic overlap and both involve cognitive impairments. Educational attainment (EDU), a key proxy for cognition, differs significantly between the two disorders. However, how the genetic architecture linking EDU to SCZ and BD diverges remains unclear. Aims & Objectives The aim of this study is to systematically investigate and compare the genetic architecture linking educational attainment (EDU) with schizophrenia (SCZ) and bipolar disorder (BD), and to elucidate the neurobiological mechanisms underlying their shared and distinct cognitive and psychiatric risk pathways. Method We utilized large-scale genome-wide association study (GWAS) summary statistics to characterize global, local, and functional genetic correlations among EDU, SCZ, and BD. Cross-trait meta-analyses, colocalization, and bidirectional Mendelian randomization (MR) were used to identify shared loci and causal relationships. Tissue- and cell-type enrichment and summary-data-based MR analyses highlighted functional convergence in brain regions. Guided by these findings, neuroimaging analysis including 50 SCZ patients, 35 BD patients, and 60 healthy controls was performed whether EDU–disorder associations were mediated by gray matter volume (GMV). Results EDU showed a stronger genetic correlation with SCZ than BD. Cross-trait meta-analysis identified 32 shared SNPs for EDU-SCZ and 8 for EDU-BD. Bidirectional MR indicated a causal association between EDU and SCZ. EDU, SCZ, and BD shared heritability enrichment in the brain cortex, prefrontal cortex, and anterior cingulate cortex, with distinct cell-type enrichments. WBP2NL and NAGA were identified as functional genes shared by EDU and SCZ across multiple brain regions. Neuroimaging analysis indicated that EDU positively associated with the GMV in the left parahippocampal gyrus which also mediated the EDU-BD relationship. Discussion & Conclusions EDU shows broader and more convergent genetic associations with SCZ, whereas in BD, its influence may operate through specific neurostructural pathways, highlighting distinct mechanisms linking cognitive potential to psychiatric vulnerability.

Read PDF

Similar papers

Open access Sep 2026

712. Comorbid mental and substance use disorders – the role of genetic susceptibility

It is demonstrated that the relationship between alcohol use and psychiatric disorders is driven by a complex, shared genetic architecture rather than environmental complications alone and underscores the value of multi-ancestry and cross-disorder genetic studies in SUD.

O. Andreassen, R. Icick, E. Wistrom et al. · 0 citations
Open access Sep 2026

666. ADHD: genes and risk for other conditions

Abstract Background Attention-deficit/hyperactivity disorder (ADHD) is a highly heritable neurodevelopmental disorder characterized by substantial clinical heterogeneity and frequent comorbidity with sleep disturbances, inflammatory conditions, and metabolic dysregulation. While ADHD has traditionally been conceptualiz...

N. Takahashi · 0 citations
Open access Aug 2026

Genomic dimensions deconstruct the clinical heterogeneity of bipolar disorder

Bipolar disorder’s genetic architecture appears hierarchical—a general liability resolving into dimensions of course and comorbidity, beyond subtypes, beyond subtypes.

Tracey van der Veen, M. Tesfaye, J. M. K. Yang et al. · 0 citations
Open access Sep 2026

Eating Disorders and Parkinson’s Disease - 2: Genetic Epidemiology and Shared Genomics

Cross-disorder AN and PD research identified shared risk variants at chr3p21.31, genes and mechanisms linked to a shared endophenotype linked to a shared endophenotype.

Andrew W. Bergen, Carolina Makowski, Michael Garvin et al. · 0 citations

We use cookies to run the site and, with your consent, for analytics and to show ads. See our Cookie Policy.